The mechanism of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis.
To determine the mechanism of hyperchloremic acidosis during recovery from diabetic ketoacidosis (DKA), serial measurements were made in eight patients of serum and urinary electrolytes and organic acids, and of urinary net acid. On admission, the average decrease in serum total CO2 was 17.5 mmol/L, corresponding to the excess anion gap, 18.5 meq/L, and the serum organic acids, 17.1 meq/L. With the treatment, the anion gap and organic acids decreased by 16.1 and 14.7 meq/L, respectively, but the serum CO2 increased only by 8.4 mmol/L; serum electrolyte balance was maintained by increase in chloride concentration. Fluid retention was insufficient to explain the disparity between the increase in CO2 and the decrease in organic acids. Renal loss of bicarbonate precursors during treatment was modest and was exceeded by renal bicarbonate production. The disparity between the increase in serum CO2 and the decrease in organic acids during treatment of DKA may be explained to a large extent by a difference in volume of distribution between bicarbonate and organic anions. The renal loss of ketone anions before admission, however, is ultimately responsible for the persistence of substantial metabolic acidosis.
D000138:Acidosis / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D002712:Chlorides / Q000097:blood*; D003920:Diabetes Mellitus / Q000378:metabolism; D016883:Diabetic Ketoacidosis / Q000378:metabolism*; D006801:Humans; D014882:Water-Electrolyte Balance
D002712:Chlorides; D002245:Carbon Dioxide